312 research outputs found
A Study On Monitoring Overhead Impact on Wireless Mesh Networks
International audienceA wireless mesh network is characterized by dynamicity. It needs to be monitored permanently to make sure its properties remain within certain limits in order to provide Quality-of-Service to the end users or to identify possible faults. To establish in every moment what is the appropriate reporting interval of the measured information and the way it is disseminated are important tasks. It has to achieve information quickly enough to solve any issue but excessive as to affect the data traffic. The problem that arises is that the monitoring information needs to travel in the network along with the user traffic and thus, potentially causing congestion. Considering that a wireless mesh network has highly dynamic characteristics there is a need for a good understanding of the influences of disseminating monitoring information in the network along with user traffic. In this paper we provide an evaluation of the network performance while monitoring information is collected from network nodes. We study how different monitoring packet sizes and different reporting frequency of the information can impact the user traffic and compare these values to the case in which only user data travels across the network
Forward Signal Propagation Learning
We propose a new learning algorithm for propagating a learning signal and
updating neural network parameters via a forward pass, as an alternative to
backpropagation. In forward signal propagation learning (sigprop), there is
only the forward path for learning and inference, so there are no additional
structural or computational constraints on learning, such as feedback
connectivity, weight transport, or a backward pass, which exist under
backpropagation. Sigprop enables global supervised learning with only a forward
path. This is ideal for parallel training of layers or modules. In biology,
this explains how neurons without feedback connections can still receive a
global learning signal. In hardware, this provides an approach for global
supervised learning without backward connectivity. Sigprop by design has better
compatibility with models of learning in the brain and in hardware than
backpropagation and alternative approaches to relaxing learning constraints. We
also demonstrate that sigprop is more efficient in time and memory than they
are. To further explain the behavior of sigprop, we provide evidence that
sigprop provides useful learning signals in context to backpropagation. To
further support relevance to biological and hardware learning, we use sigprop
to train continuous time neural networks with Hebbian updates and train spiking
neural networks without surrogate functions
Prototyping Telematic Services in a Wireless Vehicular Mesh Network Environment
International audienceNext generation telematic services are expected to play a key role in future automotive applications. In order to achieve strong integration between the services and the underlying network infrastructure there is a need for both simulation and emulation of the entire system. This paper presents a combined simulation and emulation approach for telematic services prototyping in an emulated wireless vehicular mesh networking environment. The ns-3 wireless mesh model, SUMO vehicular mobility model and different telematic services are integrated to demonstrate high scalability and flexibility of the proposed approach
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Using the Gibbs Function as a Measure of Human Brain Development Trends from Fetal Stage to Advanced Age
We propose to use a Gibbs free energy function as a measure of the human brain development. We adopt this approach to the development of the human brain over the human lifespan: from a prenatal stage to advanced age. We used proteomic expression data with the Gibbs free energy to quantify human brain’s protein–protein interaction networks. The data, obtained from BioGRID, comprised tissue samples from the 16 main brain areas, at different ages, of 57 post-mortem human brains. We found a consistent functional dependence of the Gibbs free energies on age for most of the areas and both sexes. A significant upward trend in the Gibbs function was found during the fetal stages, which is followed by a sharp drop at birth with a subsequent period of relative stability and a final upward trend toward advanced age. We interpret these data in terms of structure formation followed by its stabilization and eventual deterioration. Furthermore, gender data analysis has uncovered the existence of functional differences, showing male Gibbs function values lower than female at prenatal and neonatal ages, which become higher at ages 8 to 40 and finally converging at late adulthood with the corresponding female Gibbs functions
Prenatal Nutritional Intervention Reduces Autistic-Like Behavior Rates Among Mthfr-Deficient Mice
The causes and contributing factors of autism spectrum disorders (ASD) are poorly understood. One gene associated with increased risk for ASD is methylenetetrahydrofolate-reductase (MTHFR), which encodes a key enzyme in one carbon (C1) metabolism. The MTHFR 677C > T polymorphism reduces the efficiency of methyl group production with possible adverse downstream effects on gene expression. In this study, the effects of prenatal and/or postnatal diets enriched in C1 nutrients on ASD-like behavior were evaluated in Mthfr-deficient mice. Differences in intermediate pathways between the mice with and without ASD-like behaviors were tested. The findings indicate that maternal and offspring Mthfr deficiency increased the risk for an ASD-like phenotype in the offspring. The risk of ASD-like behavior was reduced in Mthfr-deficient mice supplemented with C1 nutrients prenatally. Specifically, among offspring of Mthfr+/- dams, prenatal diet supplementation was protective against ASD-like symptomatic behavior compared to the control diet with an odds ratio of 0.18 (CI:0.035, 0.970). Changes in major C1 metabolites, such as the ratios between betaine/choline and SAM/SAH in the cerebral-cortex, were associated with ASD-like behavior. Symptomatic mice presenting ASD-like behavior showed decreased levels of GABA pathway proteins such as GAD65/67 and VGAT and altered ratios of the glutamate receptor subunits GluR1/GluR2 in males and NR2A/NR2B in females. The altered ratios, in turn, favor receptor subunits with higher sensitivity to neuronal activity. Our study suggests that MTHFR deficiency can increase the risk of ASD-like behavior in mice and that prenatal dietary intervention focused on MTHFR genotypes can reduce the risk of ASD-like behavior
Differential Proliferative Characteristics of Alveolar Fibroblasts in Interstitial Lung Diseases: Regulative Role of IL-1 and PGE2
Fibroblasts (Fb) from patients with sarcoidosis (SA) and
hypersensitivity pneumonitis (HP) exhibited a lower proliferative
capacity compared with Fb obtained from control (CO) and diffuse
interstitial fibrosis patients (DIF). Proliferation of Fb from SA or
lip patients was suppressed by autologous LPS-stimulated alveolar
macrophages (AM) supernatants but not by those from CO patients.
Similarly, alveolar macrophages (AM) derived supernatant, obtained
from CO, did not suppress the proliferation of SA and HP Fb. AM from
SA and HP patients secreted higher amounts of IL-1α and β
compared with controls and compared with Fb from SA and HP patients.
Steady levels of IL-1α and βmRNA were expressed in
unstimulated and stimulated cultures. Fb from SA and HP patients
could be stimulated by LPS to secrete significantly higher levels of
PGE2 than those detected in supernatants from LPS
stimulated Fb of DIF patients. Only the proliferation of Fb from SA
and HP patients was sensitive to amounts of IL-1 equivalent to those
detected in the lung of these diseases. As SA and HP are two
diseases where irreversible deterioration occurs in only 20%
of the patients, we hypothesize that mediators in the lung may
modulate Fb proliferation. IL-1 of AM origin and PGE2 of
Fb origin secreted at high levels, may be candidates for this
suppression because it was abrogated by anti IL-1β and indomethacin
Detection of HER2 amplification in circulating free DNA in patients with breast cancer.
BACKGROUND: Human epidermal growth factor receptor 2 (HER2) is amplified and overexpressed in 20-25% of breast cancers. This study investigated circulating free DNA (cfDNA) for detection of HER2 gene amplification in patients with breast cancer. METHODS: Circulating free DNA was extracted from plasma of unselected patients with primary breast cancer (22 before surgery and 68 following treatment), 30 metastatic patients and 98 female controls using the QIAamp Blood DNA Mini Kit (Qiagen). The ratio of HER2 to an unamplified reference gene (contactin-associated protein 1 (CNTNAP1)) was measured in cfDNA samples by quantitative PCR (qPCR) using SK-BR-3 cell line DNA as a positive control. RESULTS: We validated the qPCR assay with DNA extracted from 23 HER2 3+ and 40 HER2-negative tumour tissue samples; the results agreed for 60 of 63 (95.2%) tumours. Amplification was detected in cfDNA for 8 of 68 patients following primary breast cancer treatment and 5 of 30 metastatic patients, but was undetected in 22 patients with primary breast cancer and 98 healthy female controls. Of the patients with amplification in cfDNA, 10 had HER2 3+ tumour status by immunohistochemistry. CONCLUSIONS: The results demonstrate for the first time the existence of amplified HER2 in cfDNA in the follow-up of breast cancer patients who are otherwise disease free. This approach could potentially provide a marker in patients with HER2-positive breast cancer
Defective microtubule-dependent podosome organization in osteoclasts leads to increased bone density in Pyk2−/− mice
The protein tyrosine kinase Pyk2 is highly expressed in osteoclasts, where it is primarily localized in podosomes. Deletion of Pyk2 in mice leads to mild osteopetrosis due to impairment in osteoclast function. Pyk2-null osteoclasts were unable to transform podosome clusters into a podosome belt at the cell periphery; instead of a sealing zone only small actin rings were formed, resulting in impaired bone resorption. Furthermore, in Pyk2-null osteoclasts, Rho activity was enhanced while microtubule acetylation and stability were significantly reduced. Rescue experiments by ectopic expression of wild-type or a variety of Pyk2 mutants in osteoclasts from Pyk2−/− mice have shown that the FAT domain of Pyk2 is essential for podosome belt and sealing zone formation as well as for bone resorption. These experiments underscore an important role of Pyk2 in microtubule-dependent podosome organization, bone resorption, and other osteoclast functions
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